Limiting intestinal iron absorption rescues glial defects and extends lifespan in a Drosophila model of Friedreich ataxia

Limiting intestinal iron absorption rescues glial defects and extends lifespan in a Drosophila model of Friedreich ataxia Ema TURKI, Estelle JULLIAN, Pierre DELAMOTTE, Anne FILIPE, Laura TIXIER CARDOSO, Sandrine MIDDENDORP, Elodie MARTIN, Veronique Monnier bioRxiv 2026.06.04.730074; doi:10.64898/2026.06.04.730074 

 Reducing intestinal iron uptake, either through treatment with bathophenanthroline disulfonic acid (BPS), an extracellular iron chelator, or by gut-specific silencing of the iron transporter Malvolio, nearly doubled fly survival. BPS treatment also improved sensitivity to dietary iron, enhanced locomotor performance, fully restored normal brain size, and prevented glial alterations. Altogether, our findings identify glial cells as early and preferential targets of frataxin deficiency in an iron-dependent manner and support the in vivo relevance of intestinal iron uptake as a potential modulator of disease severity in FRDA.

Limiting intestinal iron absorption rescues glial defects and extends lifespan in a Drosophila model of Friedreich ataxia